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Expression data from vehicle and adrenomedullin treated human lymphatic endothelial cells

ABSTRACT: Human dermal lymphatic endothelial cells were cultured and treated with either vehicle or 10 nM AM for 15 minutes, 1 hour, or 24 hours to assess gene expression changes across the human genome with AM treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE59938 | GEO | 2014/07/31

SECONDARY ACCESSION(S): PRJNA257095

REPOSITORIES: GEO

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Expression data from vehicle and adrenomedullin treated human lymphatic endothelial cells

Project description:Human dermal lymphatic endothelial cells were cultured and treated with either vehicle or 10 nM AM for 15 minutes, 1 hour, or 24 hours to assess gene expression changes across the human genome with AM treatment. Two variable experiment, time (0.25, 1, 24 hours) and treament (vehicle vs adrenomedullin) of gene expression in human lymphatic endothelial cells. Biological replicates: 3-4 per condition.

2014-07-31 | E-GEOD-59938 | biostudies-arrayexpress

Dermal lymphatic endothelial cell response to type 2 diabetes [Homo sapiens]

Project description:Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. The positively and negatively correlated dLEC transcripts directly cohere to prolonged inflammatory periods and reduced infectious resistance of patientsÂ´ skin. Further, lymphatic vessels might be involved in tissue remodeling processes during T2D induced skin alterations associated with impaired wound healing and altered dermal architecture. Hence, dermal lymphatic vessels might be directly associated with T2D disease promotion. Global gene expression profile of normal dermal lymphatic endothelial cells (ndLECs) compared to dermal lymphatic endothelial cells derived from type 2 diabetic patients (dLECs).Quadruplicate biological samples were analyzed from human lymphatic endothelial cells (4 x diabetic; 4 x non-diabetic). subsets: 1 disease state set (dLECs), 1 control set (ndLECs)

2012-06-01 | E-GEOD-38396 | biostudies-arrayexpress

Lymphatic endothelial cells comparison gene array data

Project description:GeneChipÂ® Mouse Gene 2.0 ST Array for C57BL/6 mouse skin dermal primary lymphatic endothelial cells (Ms LEC) and mouse lymphatic endothelial cell line SVEC4-10 GeneChipÂ® Human Gene 2.0 ST Array for human primary lymphatic endothelial cells (Hu LEC) Total RNA from lymphatic cell line SVEC4-10 were used for GeneChipÂ® Mouse Gene 2.0 ST Array. SVEC4-10 samples, human and mouse LEC samples.

2016-07-20 | E-GEOD-84551 | biostudies-arrayexpress

RNA-Seq of Human Dermal Lymphatic Endothelial Cells

Project description:Transcriptome exploration of Human Dermal Lymphatic Endothelial Cells

2024-04-01 | E-MTAB-13907 | biostudies-arrayexpress

Lymphatic endothelial cells comparison gene array data

Project description:GeneChip® Mouse Gene 2.0 ST Array for C57BL/6 mouse skin dermal primary lymphatic endothelial cells (Ms LEC) and mouse lymphatic endothelial cell line SVEC4-10 GeneChip® Human Gene 2.0 ST Array for human primary lymphatic endothelial cells (Hu LEC) Total RNA from lymphatic cell line SVEC4-10 were used for GeneChip® Mouse Gene 2.0 ST Array.

2016-07-20 | GSE84551 | GEO

Transcription profiling of human lymphatic endothelial cells, mouse dermal cells and human skin cells reveals an inflammation-induced mechanism for leukocyte transmigration of lymphatic vessel endothelium.

Project description:The exit of antigen-presenting cells (APC) and lymphocytes from inflamed skin to afferent lymph is vital for the initiation and maintenance of dermal immune responses. How such exit is achieved and how cells transmigrate the distinct endothelium of lymphatic vessels is however unknown. Here we show that inflammatory cytokines trigger activation of dermal lymphatic endothelial cells (LEC) leading to expression of the key leukocyte adhesion receptors ICAM-1, VCAM-1 and E-selectin, as well as a discrete panel of chemokines and other potential regulators of leukocyte transmigration. Furthermore, we show that both ICAM-1 and VCAM-1 are induced in the dermal lymphatic vessels of mice exposed to skin contact hypersensitivity where they mediate lymph node trafficking of DC via afferent lymphatics. Lastly, we show that TNF_-stimulates both DC adhesion and transmigration of dermal LEC monolayers in vitro and that the process is efficiently inhibited by ICAM-1 and VCAM-1 adhesion-blocking mAbs. These results reveal a CAM-mediated mechanism for recruiting leukocytes to the lymph nodes in inflammation and highlight the process of lymphatic transmigration as a potential new target for anti-inflammatory therapy. Experiment Overall Design: Global gene expression profile of normal dermal lymphatic endothelial cells cultured in media alone (no TNF) compared to that of normal dermal lymphatic endothelial cells stimulated with TNFalpha, 1 ng/ml for 48h.Triplicate biological samples were analyzed from human lymphatic endothelial cells (3 x controls; 3 x TNF treated) and a single sample analyzed from mouse lymphatic endothelial cells (1 x controls; 1 x TNF treated).

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RNA Sequencing of primary human dermal microvascular blood and lymphatic endothelial cells

Project description:Human dermal microvascular blood and lymphatic endothelial cells display distinct transcriptomic landscape.

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ChIP Sequencing of primary human dermal microvascular blood and lymphatic endothelial cells

Project description:Human dermal microvascular blood and lymphatic endothelial cells manifest unique profiles of histone modifications.

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Dermal lymphatic endothelial cell response to type 2 diabetes [Homo sapiens]

Project description:Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. The positively and negatively correlated dLEC transcripts directly cohere to prolonged inflammatory periods and reduced infectious resistance of patients´ skin. Further, lymphatic vessels might be involved in tissue remodeling processes during T2D induced skin alterations associated with impaired wound healing and altered dermal architecture. Hence, dermal lymphatic vessels might be directly associated with T2D disease promotion.

2012-06-02 | GSE38396 | GEO

Immune-interacting lymphatic endothelial subtype at capillary terminals drives lymphatic malformation

Project description:Oncogenic mutations in PIK3CA, encoding p110α-PI3K, are a common cause of venous and lymphatic malformations. Vessel type-specific disease pathogenesis is poorly understood, hampering development of efficient therapies. Here, we reveal a new immune-interacting subtype of Ptx3-positive dermal lymphatic capillary endothelial cells (iLECs) that recruit pro-lymphangiogenic macrophages to promote progressive lymphatic overgrowth. Mouse model of Pik3caH1047R-driven vascular malformations showed that proliferation was induced in both venous and lymphatic ECs, but sustained selectively in LECs of advanced lesions. Single-cell transcriptomics identified the iLEC population, residing at lymphatic capillary terminals of normal vasculature, that was expanded in Pik3caH1047R mice. Expression of pro-inflammatory genes, including monocyte/macrophage chemokine Ccl2, in Pik3caH1047R-iLECs was associated with recruitment of VEGF-C-producing macrophages. Macrophage depletion, CCL2 blockade or anti-inflammatory COX-2 inhibition limited Pik3caH1047R-driven lymphangiogenesis. Thus, targeting the paracrine crosstalk between iLECs and macrophages provides a new therapeutic opportunity for lymphatic malformations. Identification of iLECs further indicates that peripheral lymphatic vessels not only respond to but also actively orchestrate inflammatory processes.

2023-01-16 | GSE201916 | GEO

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